I guess what I am trying to say is this, if slow adult onset Type 1 happens as a gradual attack, a slow destruction of beta cells , slow enough that replication of beta cells can still take place, small skirmishes if you will with moments of re-grouping (honeymoon period). Against an all out war and total massacre of beta cells with no replenishing taking place in child onset type 1. There is no instability as the entire kit and caboodle has been wiped out. And Type 2 which is a process failure with the eventual long term burnout of beta cells but relatively stable pancreas secretion.
In short is your pancreas, for the time being, still secreting insulin in a stable manner or, due to your body’s autoimmune responses, made your pancreas unstable in its secretion of insulin and, therefore, difficult to manage? I guess that’s my point. And I totally accept that it could just be down to insulin management.